Epithelial type II cells of the pulmonary alveolus synthesize and secrete surface active material (SAM). This substance is apparently required for normal lung functionabsence of SAM results in alveolar collapse and diffuse atelectasis. Deficiencies of SAM are thought to be responsible for the etiology of neonatal and perhaps adult respiratory distress syndrome. Physiologic and biochemical data also suggest that a decrease or an inactivation of SAM is responsible for some of the physiologic changes that are seen in the aged lung (i.e., early closure of peripheral airways at relatively high lung volumes). Type II cells will be isolated from the lung with trypsin and separated from other lung cells with discontinuous density gradients. The isolated cells will then be put into primary culture. As with other epithelial cells, normal functional and morphologic characteristics of type II cells deteriorate as the cells are kept in culture. Type II cells have an active lysosome system and it is likely that deteriorative changes which are observed in the cultured cells are partly a result of lysosome-induced changes. Thus far, type II cells have been cultured under relatively simple conditions. Major aspects of the culture system such as serum type and concentration and the physical substrate upon which the cells attach will be altered. This will provide a culture environment that will be more conducive to maintaining the normal functional and morphologic characteristics of type II cells. As type II cells respond favorably to improvements in the culture environment, changes in certain lysosomal characteristics will be measured to determine if maintenance of differentiated function in cultured type II cells is related to changes in lysosomal functions. These data will provide information about those processes which might occur as type II cells degenerate in culture and might provide further insight into senescence related changes of lung function as the lung ages in vivo.